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343 mt > DRUG INDUCED KIDNEY INJURY > Flashcards

DRUG INDUCED KIDNEY INJURY Flashcards

1
Q

EPIDEMIOLOGY - read

A

▪ Nephrotoxic drugs were contributing factors in 19-25% of cases of severe
acute kidney injury
▪ Older adults – as high as 66%
▪ Common complication of several diagnostic and therapeutic agents
▪ Source of significant morbidity and mortalit

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2
Q

drugs causing Prerenal/Hemodynamic injury

A

ACE inhibitors/ARBs
NSAIDS
Calcineurin inhibitors

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3
Q

drugs causing intrinsic injury

  • acute tubular necrosis
  • acute interstital nephritis
  • chronic interstital nephritis
A

Acute Tubular Necrosis
Amphotericin B
Aminoglycosides
Radiographic Contrast Dye

Penicillins
Lithium

Calcineurin inhibitors

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4
Q

drugs causing Obstructive (Post renal) injury

A

Acyclovir
Indinavir
Sulfonamide antibiotics

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5
Q

see slide 45 for autoregulation

A

ok

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6
Q

ACE INHIBITORS/ARBS HEMODYNAMIC (PRERENAL) RENAL FAILURE

which pts are at higher risk?

A

Patients at higher risk:
▪ Patients with severe atherosclerotic disease
▪ Renal artery stenosis (bilateral)
▪ Heart Failure (acute, decompensated)
▪ Chronic Kidney Disease (severe later stages)
▪ Volume depleted

Examples ▪ ACEI: Ramipril, Lisinopril, Perindopril
▪ ARBS: Telmisartan, irbesartan, valsartan

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7
Q

ACE INHIBITORS/ARBS HEMODYNAMIC (PRERENAL) RENAL FAILURE

presentation?
how does it work?

A

▪ ≥ 30% rise in serum creatinine within 2 to 7 days following initiation of therapy
▪ Usually stabilizes within 1 week

Mechanism
▪ Normally, in cases of decreased renal blood flow, intraglomerular blood pressure is maintained by vasodilation of the afferent arteriole and vasoconstriction of the efferent arteriole
▪ ACE inhibitors dilate the efferent arteriole and thus reduce glomerular hydrostatic
pressure = ↓ GFR

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8
Q

ACE INHIBITORS/ARBS HEMODYNAMIC (PRERENAL) RENAL FAILURE

urine findings
- volume, conc, FeNa, BUN, creatine
management?

A 
▪ Low urine volume
▪ Low urine sodium concentration (< 20 mmol/L)
▪ FeNa <1%
▪ Urinalysis: relatively normal
▪ Specific gravity >1.010
▪ No casts or cellular elements
▪ High BUN, High Creatinine
▪ Management
▪ d/c ACE inhibitor or ARB
▪ Supportive therapy
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9
Q

ACE INHIBITORS/ARBS HEMODYNAMIC (PRERENAL) RENAL FAILURE

prevention

A

▪ Prevention
▪ Obtain baseline SCR and K+
▪ Start with low doses, titrate dose gradually
▪ Avoid other drugs which may alter renal blood flow
▪ NSAIDS
▪ Maintain hydration
▪ Monitor SCr and K+ regularly
▪ Temporarily stop drugs in the setting of “stressed” kidneys

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10
Q

NSAIDS HEMODYNAMIC (PRERENAL) RENAL FAILURE

which pts at higher risk?
which NSAID will most likely impair renal fxn?

A 
▪ Patients at higher risk:
▪ Chronic Kidney disease
▪ Heart failure
▪ Elderly
▪ ACE Inhibitor/NSAID combination

▪ Indomethacin is most likely to impair renal function
▪ Low dose Aspirin does not impair renal function!

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11
Q 
NSAIDS  HEMODYNAMIC (PRERENAL) RENAL FAILURE
presentation?
mechanism?

see slide 54!

A

Presentation
▪ Patients present with low urine volume, edema/weight gain and elevated SCr, K+,
and BUN

Mechanism
▪ In patients with altered renal perfusion, the compensatory response is to release
PGs. Inhibition of COX-2 inhibits this prostaglandin response. NSAIDS, therefore,
inhibit afferent arterial dilation and reduce GFR

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12
Q

NSAIDS HEMODYNAMIC (PRERENAL) RENAL FAILURE

urine findings
- volume, conc, FeNa, BUN, creatine

A 
▪ Urine Findings 
▪ Low urine volume 
▪ Low urine sodium (<20mmol/L) 
▪ FeNa <1% 
▪ Urinalysis: relatively normal 
▪ ↑ SG 
▪ No casts or cellular debris

▪ High BUN, High Creatinine

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13
Q

NSAIDS HEMODYNAMIC (PRERENAL) RENAL FAILURE

management and prevention

A

▪ Management
▪ d/c offending agent
▪ Supportive therapy

▪ Prevention
▪ Avoid NSAID use in elderly, HF, CKD
▪ Avoid concomitant use with ACEI or ARB
▪ Start with low doses and titrate slowly
▪ Monitor BP, SCr, and BUN regularly
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14
Q

ACUTE TUBULAR NECROSIS (ATN)

A

▪ Most common form of intrarenal acute kidney injury.
▪ Precipitating factors include ischemic and nephrotoxic processes.
▪ Clinical course is highly variable
▪ Oliguric phase: Within 24 hours and lasting 1-3 weeks
▪ Diuretic phase: Usually indicates renal recovery
▪ Mortality rates range from 50-70%
▪ Complete recovery of renal function may not return

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15
Q

ATN causes

A 
Nephrotoxic ATN
▪ Endogenous or exogenous
▪ Myoglobin
▪ Aminoglycosides (gentamicin, tobramycin)
▪ CT Contrast Dye

Sepsis associated ATN
▪ Ischemia and toxin related

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16
Q

ATN - AMINOGLYCOSIDES

which pts at high risk?

A

▪ Gentamicin, tobramycin

Patients at high risk
▪ Dehydrated
▪ Sepsis, ischemia
▪ Pre-existing renal impairment
▪ Concomitant nephrotoxins
▪ Sustained high AG serum levels and large cumulative doses
▪ Long term AG therapy (> 14 days)

Presentation
▪ ↑ SCr 6-10 days

17
Q

ATN - AMINOGLYCOSIDES

mechanism

A

▪ Epithelial cell damage in proximal tubular cells
▪ Direct signaling of cell death of proximal tubule cells
▪ Toxicity related to cationic charge
▪ Neomycin>gentamicin/tobramycin>amikacin>streptomycin

18
Q

ATN - AMINOGLYCOSIDES

urine findings

A 
▪ Muddy brown epithelial cell casts and free epithelial cells
▪ High urine sodium (> 40 mmol/L)
▪ FeNa >3%
▪ Urinalysis
▪ Specific Gravity ~1.010
19
Q

ATN - AMINOGLYCOSIDES

management and prevention

A 
Management
▪ D/C aminoglycoside
▪ Supportive therapy
▪ Correct volume derangements
▪ Correct metabolic acidosis
▪ Hemodialysis/Renal Replacement Therapy
Prevention
▪ Avoid hypovolemia
▪ Avoid prolonged therapy
▪ Therapeutic drug monitoring
▪ Avoid other nephrotoxins
▪ Alternate dosing strategies
▪ Avoid high risk populations – elderly, pre-existing renal impairment
20
Q

ACUTE INTERSTITIAL NEPHRITIS

presentation

A

▪ Up to 3% of all cases of acute kidney injury

Presentation
▪ Fever
▪ Rash
▪ Pyuria/hematuria
▪ Oliguria
▪ Other
▪ Metabolic acidosis
▪ Hyperkalemia
▪ Salt wasting
▪ Occur ~ 14 days after exposure to drug
21
Q

ACUTE INTERSTITIAL NEPHRITIS

mechanism

A

▪ Hypersensitivity reaction

▪ Lymphocytic infiltration of the interstitium

22
Q

ACUTE INTERSTITIAL NEPHRITIS
urine findings
implicated drugs (2)

A 
▪ WBC (pyuria)
▪ FeNa >1%
▪ Urine Na > 40mmol/L
▪ Hematuria
▪ White cell casts
▪ Mild proteinuria
▪ Eosinophils

▪ Implicated drugs: penicillins, lithium (Chronic Interstitial Nephritis)

23
Q

ACUTE INTERSTITIAL NEPHRITISS

management

A 
▪ Management
▪ D/C offending drug
▪ Supportive therapy
▪ Correct volume derangements
▪ Prednisone therapy for up to 4 weeks
▪ Intermittent hemodialysis
24
Q

OBSTRUCTIVE NEPHROPATHY

3 presentations

A

▪ Refers to problems in the ureters, bladder and urethra
▪ Must be in both kidneys

3 presentations
▪ Renal tubular obstruction
▪ Extrarenal urinary tract obstruction
▪ Nephrolithiasis (kidney stones)

25
Q

OBSTRUCTIVE NEPHROPATHY

pts at high risk

A

▪ Volume depleted
▪ Underlying renal insufficiency
▪ Concomitant metabolic disorders

26
Q

OBSTRUCTIVE NEPHROPATHY

explain
▪ Renal tubular obstruction
▪ Extrarenal urinary tract obstruction
▪ Nephrolithiasis (kidney stones)

which drugs cause them?

A

Renal Tubular Obstruction
▪ Intratubular precipitation of drug crystals or other tissue degradation products
▪ Ex: acyclovir, rhabdomyolysis with statins

Extrarenal urinary tract obstruction
▪ Males with BPH given anticholinergic drugs

Nephrolithiasis
▪ Precipitation of stone forming components into ureters
▪ Indinavir

27
Q

OBSTRUCTIVE NEPHROPATHY

urine findings

management

A 
Urine Findings
▪ Red/white blood cells
▪ Crystals
▪ Acyclovir – needle shaped
▪ Indinavir – rectangular plates or rosettes
Management
▪ d/c offending drug
▪ Hydration
▪ Loop diuretic
▪ Supportive therapy
28
Q

OBSTRUCTIVE NEPHROPATHY

prevention

A

▪ Aggressive hydration
▪ Avoid rapid infusions and large bolus doses of acyclovir
▪ Urine alkalinization

29
Q

DRUG-INDUCED STONES

risk factors

A 
● 1-2 % of all stones
● Risk Factors
▪ Daily dose
▪ Duration of treatment
▪ Urinary excretion of drug or metabolite
▪ Solubility of drug or metabolite
▪ Concentration peaks in the urine – rate of elimination
▪ Morphology of the crystals
30
Q

DRUG INDUCED STONES - CAUSES

which drug classes cause crystallization in urine?

A

● Crystallize in the urine
▪ Antibacterials – sulphonamides, cephalosporins, quinolones, furanes, pyridines,
aminopenicillins
▪ Protease inhibitors (indinavir, nelfinavir, acyclovir)
▪ Antihypertensives (triamterene)
▪ Others: primidone, methotrexate, guaiafenisin, allopurinol, sulfasalazine

31
Q

DRUG INDUCED STONES - CAUSES

which drug classes cause metabolically induced in urine?

A

● Metabolically induced
▪ Change in fluid balance – furosemide, corticosteroids, laxative abuse
▪ Change pH – carbonic anhydrase inhibitors, carbonate/bicarbonates, alkalinizing agents, acidifying drugs
▪ Hypercalciuria – calcium and vitamin D supplements, furosemide,
corticosteroids
▪ Hypophosphatemia – aluminum hydroxide
▪ Hyperoxaluria – Vitamin C, urcosurics, antibacterials

343 mt (15 decks)

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